Estrogen priming affects the sensitivity of midbrain central gray neurons to microiontophoretically applied LHRH but not beta-endorphin.

Abstract

In vivo single-unit extracellular recording was used to assess neuronal membrane sensitivity at the level of the midbrain central gray (MCG) to the iontophoresis of luteinizing hormone releasing hormone (LHRH) and beta-endorphin (beta-END). The percentage of change in firing rate was evaluated to determine the effect of exogenously administered estradiol benzoate (EB) and EB plus progesterone (EB + P) on the membrane sensitivity of these MCG neurons to LHRH and beta-END. Ovariectomized adult female rats were primed with EB or EB + P, or nonprimed, 24-48 h prior to recording. EB priming significantly altered the membrane sensitivity of neurons in the MCG to LHRH by increasing the number of cells excited compared to the EB + P group and the nonprimed controls (p less than 0.005). The addition of P appeared to negate this effect. Hormonal priming did not alter the response profile for beta-END iontophoresis. The results suggest an estrogen-dependent sensitivity to LHRH at the MCG which translates into an increased electrical output, ultimately facilitating lordosis behavior. P treatment dampens this excitation. beta-END's effect on neuronal membrane excitability at the MCG was not distinctly characterized under the hormonal conditions our study evaluated and may reflect a regulatory role under physiological extremes.